Acute Hepatitis: Swelling and Apoptosis Piecemeal or Bridging, panacinar necrosis Inflammation – lymphocytes, Macrophages Ground glass hepatocytes – HBV Mild fatty change – HCV Portal inflammation and Cholestasis
Fulminant Hepatitis: Hepatic failure with in 2-3 weeks. Reactivation of chronic or acute hepatitis Massive necrosis, shrinkage, wrinkled Collapsed reticulin network Only portal tracts visible Little or massive inflammation – time More than a week – regenerative activity
Alcoholic Liver Injury: Ethyl alcohol : Common cause of acute/Chronic liver disease Alcoholic Liver disease - Patterns Fatty change, Acute hepatitis (Mallory Hyalin) Chronic hepatitis with Portal fibrosis Cirrhosis, Chronic Liver failure All reversible except cirrhosis stage.
Alcoholic Liver Injury: Pathogenesis Acetaldehyde – metabolite – hepatotoxic Diversion of metabolism – fat storage. Oxidation of ethanol NAD to NADH. NAD is required for the oxidation of fat.. Increased peripheral release of fatty acids. Inflammation, Portal bridging fibrosis Stimulates collagen synthesis – fibrosis. Micronodular cirrhosis.
Definition:1. Diffuse disorder of liver characterised by;2. Complete loss of normal architecture,3. Replaced by extensive fibrosis with,4. Regenerating parenchymal nodules.
Introduction Cirrhosis is common end result of many chronic liver disorders. Diffuse scarring of liver – follows hepatocellular necrosis of hepatitis. Inflammtion – healing with fibrosis - Regeneration of remaining hepatocytes form regenerating nodules. Loss of normal architecture & function.
Bleeding in Liver disease: vitamin K – in liver gamma-carboxyglutamic acid – for coagulation factors II, VII, IX, and X. Liver disease factor VII is the first to go so the defect will appear initially in the extrinsic pathway, i.e., abnormal PT. When severe it affects both pathways.